Erythrocytes change their micromechanical properties associated with membrane viscoelasticity when they perform the transport function. There is some evidence that this is due to the influence of signaling molecules, including such gasotransmitters as nitrogen oxide (NO) and hydrogen sulfide (H2S). The aim of this study was to investigate the changes in microrheology of human erythrocytes under the influence of donors and stimulants of endogenous formation of gasotransmitters. The erythrocyte deformability, assessed by the elongation index of erythrocytes (EIE), and aggregation parameters, the indices of aggregation of erythrocytes (IAE), of washed cells were recorded after their incubation with sodium nitroprusside (SNP); sodium hydrosulfide (NaHS), the donor of H2S; 1H-[1,2,4]-oxadiazolo [4,3-a] quinoxalin-l-one (ODQ), an inhibitor of soluble guanylate cyclase; L-arginine and N-nitroarginine methyl ester (L-NAME), a substrate and an inhibitor of NO synthase, respectively; and glibenclamide (GBC ), the blocker of ATP-sensitive potassium channels. In addition, the resealed ghosts of erythrocytes were prepared, incubated with the above compounds, and the change in their deformability was evaluated. EIE increased by 8–11% (p < 0.01) and IAE decreased by 11–26% (p < 0.01) after the incubation of erythrocytes with SNP and NaHS, respectively. L-arginine and SNP exerted similar microrheological effects, which were eliminated by L-NAME or ODQ. GBC caused an increase in EIE by 8% (p < 0.05); the effects of GBC and NaHS were not additive. Incubation of the erythrocyte ghosts with SNP, L-arginine and NaHS was accompanied by a moderate but significant increase in membrane elasticity (p < 0.05). The obtained results indicate that the donors and stimulators of gasotransmitters NO and H2S moderately increase deformability of erythrocytes and markedly reduce their aggregability. The experiments on the erythrocyte ghosts suggest the existence of a direct effect of gasotransmitters on the viscoelastic properties of the membrane of these cells, which is independent of cGMP.

中文翻译：

---

气体递质对红细胞膜弹性和微流变学的影响

红细胞在执行转运功能时会改变与膜粘弹性相关的微机械特性。有一些证据表明，这是由于信号分子的影响，包括诸如氮氧化物 (NO) 和硫化氢 (H2S) 之类的气体发射体。本研究的目的是研究在供体和气体递质内源性形成刺激剂的影响下人类红细胞微流变学的变化。在与硝普钠 (SNP) 孵育后记录洗涤细胞的红细胞变形能力, 通过红细胞伸长指数 (EIE) 和聚集参数、红细胞聚集指数 (IAE) 进行评估; 硫氢化钠 (NaHS)，H2S 的供体；1H-[1,2,4]-恶二唑并 [4,3-a] 喹喔啉-l-酮 (ODQ)，可溶性鸟苷酸环化酶抑制剂；L-精氨酸和 N-硝基精氨酸甲酯 (L-NAME)，分别是 NO 合酶的底物和抑制剂；和格列本脲 (GBC)，ATP 敏感钾通道的阻滞剂。此外，制备重新密封的红细胞血影，与上述化合物一起温育，并评价其变形能力的变化。红细胞分别与 SNP 和 NaHS 孵育后，EIE 增加了 8-11% (p < 0.01)，IAE 减少了 11-26% (p < 0.01)。L-精氨酸和 SNP 具有相似的微流变学效应，但被 L-NAME 或 ODQ 消除。GBC 导致 EIE 增加 8% (p < 0.05)；GBC 和 NaHS 的影响不相加。用 SNP 孵育红细胞影，L-精氨酸和 NaHS 伴随着膜弹性的适度但显着增加（p < 0.05）。所得结果表明气体递质NO和H2S的供体和刺激物适度增加红细胞的变形能力并显着降低其聚集能力。红细胞影的实验表明，气体递质对这些细胞膜的粘弹性有直接影响，这与 cGMP 无关。